CHICKENPOX(Varicella)

Dr.K.R.RahulDept. of Swasthavritta.Amrita School of Ayurveda.

CHICKENPOX

How it got its name?

Also known as Varicella

The first documented use of the term chicken pox was in 1684

Chicken pox is an acute highly infectious disease.

Caused by the varicella – Zoster virus (VZV).

Primary infection results in Varicella.

Characterized by the vascular rash, that may be accompanied by the fever and malaise.

World wide in distribution occurs both as endemic and epidemic form.

AGENT FACTORS

Agent

Varicella – Zoster Virus

Human α Herpes virus type III

VZV is a DNA virus

A member of Herpes virus group.

Primary infection causes chickenpox followed by

Latent infection in cranial nerves sensory ganglia

and spinal dorsal root ganglia.

Latent infection causes painful, vesicular ,pustular

eruption in the distribution of one or more sensory nerve roots.

AGENT FACTORS

Source of infection

Oropharyngeal secretion

Lesion of the skin and mucosa

Rarely patients with Herpes Zoster .

Virus can be isolated from the vesicular fluid during the first 3days of illness

Infectivity

period of communicability- 1 to 2days before and 4 to 5 days after appearance of rash.

Infectivity ceases once the lesions are crusted.

Virus tend to die out before pustular stage.

Secondary attack rate

Chickenpox is highly communicable

Secondary attack rate in household contact is up to 90%

HOST FACTORS

Age

Occurs primarily in children under 10yrs.

Disease can be severe in adults.

Immunity

One attack gives durable immunity.

Maternal antibodies protects infant during first few months.

Cell mediated immunity helps in the recovery from VZV.

IgG antibodies persist for life time and prevents from varicella.

HOST FACTORS

Pregnancy

The dangers to the foetus associated with a primary VZV infection are greater in the first six months.

In 3rd trimester mother is more likely to have severe symptoms.

Maternal infection is associated with premature delivery.

Infection leads to congenital varicella syndrome.

Effects on the foetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation.

ENVIRONMENTAL FACTORS

Chickenpox shows a seasonal trend in India, mostly occur in first 6months of the year.

In temperate climates there is little evidence of seasonal trends.

TRANSMISSION

Transmitted from person to person by droplet infection via droplet nuclei.

Portal of entry is through respiratory tract.

Fomites doesn’t play a significant role in transmission.

Virus can cross the placenta and cause congenital varicella.

Chickenpox can also be spread from people with shingles.

INCUBATION PERIOD

Usually 14 to 16 days, 10 to 21 days are also reported

CLINICAL FEATURES

Vary from mild illness to severe febrile illness with wide spread rashes.

Mild prodromal (fever, malaise) for 1-2 days

Successive crops (2-4 days) of pruritic vesicles

Generally appear first on head; most concentrated on trunk

Can spread over the entire body causing between 250 to 500 itchy blisters

Generally mild in healthy children

Divided into 2 stages

a) PRE-ERUPTIVE STAGE

b) ERUPTIVE STAGE

PRE-ERUPTIVE STAGE

Sudden onset with mild or moderate fever.

Headache, backache and sore throat.

In children this stage is very brief (about 24hrs).

In adults the illness is more severe and last for2 to 3 days.

ERUPTIVE STAGE

In children the rash is often first sign coming on the day the fever starts.

The distinctive features of rash are:

Centripetal Distribution

Rapid Evaluation

Pleomorphism

Fever

ERUPTIVE STAGE

Distribution

Rash is symmetric.

Centripetal in distribution.

a.First appears on the trunk (abundant)

b.Then to face, arms and legs (less abundant)

Mucosal surface are generally involved.

Axilla may be affected. But palms and soles are not affected.

Density diminishes centrifugally.

ERUPTIVE STAGE

Rapid evolution

Rash advances quickly through the stage of the macule, papule, vesicles and scab

Vesicles are dew – drops like in appearance, present on the skin, containing the clean fluid superficial in site, with the easily ruptured wall and surrounded by the area of the inflammation and are not umblicated.

The vesicles may form the crusts without going through the pustular stage

Scabbing begin 4 – 7 days after the rash appearance

ERUPTIVE STAGE

Pleomorphism

All stages of the rash (Papule, vesicles & crusts) may be seen simultaneously at one time in same area.

This due to the rash appearing in the successive crops for the 4 – 5 days in same area.

Fever

The fever does not run high.

Temperature rises with each fresh crop of rash.

smallpox chickenpox

1.Incubation period 12days(7-17days) 15days(7-21days)

2.Prodromal symptoms Severe Usually mild

3.Distribution of rash • Centrifugal• Palms and soles involved.• Axilla usually free.• Predominant on extensor & bony

prominence.

• Centripetal• Rarely affected.• Axilla affected.• Mostly on flexor surface.

4.Characteristics of rash • Deep-seated.• Vesicles multilocular & umbilicated.• Only one stage of rash seen.• No area of inflammation around vesicle

• Superficial.• Unilocular & unumbilicated.• Pleomorphic.• Area of inflammation around rash

seen.

5.Evolution of rash • Slow deliberate and majestic passing through definite stage.

• Scab formed in 10-14 days after rash appears.

• Evolution of rashes very rapid.

• Forms in 4-7days after the rash appears.

6.fever • Subsides with the appearance of rash, but may rise again in the pustular stage.

• Temperature rises with each fresh crop of rash.

COMPLICATION

Chickenpox is mild and self limiting disease.

In uncomplicated cases mortality less than 1%.

Severe complication occur in immunosuppressed patients and may occur in normal children and adults.

Hemorrhage (varicella haemorrhagica)

Pneumonia.

Encephalitis.

Acute cerebellar Ataxia.

Reye’s Syndrome

Fetal death and birth defects in case of the maternal varicella during the pregnancy.

Acute retinal necrosis and progressive outer retinal necrosis in AIDS patients.

COMPLICATION

The most common complications are:

Bacterial infections of the skin and soft tissues in children

Septicaemia

Toxic Shock Syndrome

Necrotizing Fasciitis

Osteomyelitis

Bacterial pneumonia

Septic arthritis.

LABORATORY DIAGNOSIS

Rarely required as clinical signs are clear-cut.

Examination of the vesicle fluid in electronic microscope shows round particles.

Used for culturing virus.

Serology is used for epidemiological surveys.

CONTROL

Usual control methods are –Notification, isolation and disinfection.

Isolation of cases for about 6 days after onset of rash.

Disinfection of articles soiled with nose and throat discharge.

Anti viral therapy against varicella – Acyclovir, Valacylovir, Famiciclovir and foscarnet.

Acyclovir- can prevent the development of systemic disease in immunocompromised patients, but it doesn’t prevent the post-herpetic neuralgia.

PREVENTION

1. VERICELLA ZOSTER IMMUNOGLOBULIN (VZIG)

Given with in 72 hrs of exposure particularly in immune suppressed person.

includes:

Susceptible person receiving immunosuppressive therapy

Congenital cellular immunodeficiency.

Acquired immunodeficiency.

Pregnant women

New-borns, premature infant with low birth weight.

VZIG has no therapeutic effect.

Dose: 12.5unit/kg body weight, maximum of 625 units, repeat dose in 3 week.

Not given along with varicella vaccine.

PREVENTION

2. Vaccine

Live attenuated varicella vaccine is used

Recommended for children between 12-18 months, who have not had chickenpox.

90% efficiency is suggested.

Should not be given to immunocompromised person, HIV positive person, pregnant women.

Thank you